In this study the synergistic role of the two haemodynamic parameters, pressure and wall shear stress, in macromolecular
transport has been examined across the wall of the rabbit thoracic aorta. Arteries were subjected to 70 and 150 cm water pressure
in the presence of fluid flow imposed shear stress. The flux of FITC labelled bovine serum albumin was found to be
3.36-1.34×10−6 and 1.99-0.77×10−6 cm/s (mean-S.D.) after 90 min incubation at 70 and 150 cm water, respectively. The
mean relative tissue concentrations were 0.0039-0.0025 and 0.012-0.007 at 70 and 150 cm water, respectively. Under low values
of steady wall shear stress, efflux of BSA is retarded at 150 cm since its tissue concentration is found to be higher than at 70 cm. The net outcome arises as a result of the interaction of increased permeability of endothelial cells exposed to shear stress, the pressure induced distension of the wall matrix and the differential effect of EDRF/NO at the two pressures on medial hydraulic conductivity. In the presence of the EDRF/NO inhibitor L-NAME, reduction in flux of albumin was observed at both the pressures, the decrease being greater at 150 cm water. In the absence of EDRF, the NO synthase independent vasodilator EDHF may be released, which maintains the tone of the medial smooth muscle low. Action of EDHF may be more marked at 150 cm water because NO synthesis is attenuated by higher transmural pressure and the presence of L-NAME eliminates shear stress stimulated NO release. Consequently the dilated vessel will have decreased porosity and less albumin space. The BSA flux across the aorta is, therefore, influenced by both endothelial permeability and permeability of the medial matrix, which are in turn
modulated by an interplay of transmural pressure and fluid flow generated shear stress.